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Biomedical subjects

Yan Chen

Publications and source records attributed to Yan Chen.

At least 55 records · Page 3Linked to original sources

Rare Earth coordination polymers with zeolite topology constructed from 4-connected building units.

A series of rare earth coordination polymers, M(BTC)(DMF)(DMSO) (M = Tb (1), Ho (2), Er (3), Yb (4), Y (5)), with zeolite ABW topology have been synthesized under mild conditions. They exhibit the same three-dimensional (3D) architecture and crystallize in monoclinic symmetry space group P2(1)/n. Their structures are built up from inorganic and organic 4-connected building units, whose vertex symbols are 4.4.6.6.6.8. The building units link to each other to generate approximate 5 x 8 angstroms2 channels along the [100] direction. The luminescent and magnetic properties of these compounds are investigated, and the results reveal that they could be anticipated to be potential antiferromagnetic and fluorescent materials.

Crystallography, X-Ray↗

High-resolution quantitative computed tomography demonstrating selective enhancement of medium-size collaterals by placental growth factor-1 in the mouse ischemic hindlimb.

BACKGROUND: The process of arteriogenesis after occlusion of a major artery is poorly understood. We have used high-resolution microcomputed tomography (mu-CT) imaging to define the arteriogenic response in the mouse model of hindlimb ischemia and to examine the effect of placental growth factor-1 (PlGF-1) on this process. METHODS AND RESULTS: After common femoral artery ligation, mu-CT imaging demonstrated formation of collateral vessels originating near the ligation site in the upper limb and connecting to the ischemic calf muscle region. Three-dimensional mu-CT and quantitative image analysis revealed changes in the number of segments and the segmental volume of vessels, ranging from 8 to 160 microm in diameter. The medium-size vessels (48 to 160 microm) comprising 85% of the vascular volume were the major contributor (188%) to the change in vascular volume in response to ischemia. Intramuscular injections of Ad-PlGF-1 significantly increased Sca1+ cells in the circulation, alpha-actin-stained vessels, and perfusion of the ischemic hindlimb. These effects were predominantly associated with an increase in vascular volume contributed by the medium-size (96 to 144 microm) vessels as determined by mu-CT. CONCLUSIONS: High-resolution mu-CT delineated the formation of medium-size collaterals representing a major vascular change that contributed to the restoration of vascular volume after ischemia. This effect is selectively potentiated by PlGF-1. Such selective enhancement of arteriogenesis by therapeutically administered PlGF-1 demonstrates a desirable biological activity for promoting the growth of functionally relevant vasculature.

Animals↗

Combination therapy with 2-difluoromethylornithine and a polyamine transport inhibitor against murine squamous cell carcinoma.

Using a recently developed autochthonous mouse model of squamous cell carcinoma (SCC), a combination therapy targeting polyamine metabolism was evaluated. The therapy combined 2-difluoromethylornithine (DFMO), an inhibitor of ornithine decarboxylase (ODC), and MQT 1426, a polyamine transport inhibitor. In 1 trial lasting 4 weeks, combination therapy with 0.5% DFMO (orally, in the drinking water) and MQT 1426 (50 mg/kg i.p., bid) was significantly more effective than with either single agent alone when complete tumor response was the endpoint. In the combination group, 72% of SCCs responded completely vs. 21 and 0% for DFMO and MQT 1426, respectively. A second trial involved a 4-week treatment period followed by 6 weeks off-treatment. With apparent cures as an endpoint, combination therapy was again more effective than either agent alone: a 50% apparent cure rate was observed in the combination group vs. 7.7% in the DFMO group. MQT 1426 had no inhibitory effect on SCC ODC activity nor did it enhance the inhibition by DFMO, but SCC polyamine levels declined more rapidly when treated with combination therapy vs. DFMO alone. The apoptotic index in SCCs was transiently increased by combination therapy but not by DFMO alone. Thus, targeting both polyamine biosynthesis and polyamine transport from the tumor microenvironment enhances the efficacy of polyamine-based therapy in this mouse model of SCC.

Animals↗

Syntheses, structures, ionic conductivities, and magnetic properties of three new transition-metal borophosphates Na5(H3O){M(II)3[B3O3(OH)]3(PO4)6}.2H2O (M(II) = Mn, Co, Ni).

Three new open-framework transition-metal borophosphates Na5(H3O){M(II)3[B3O3(OH)]3(PO4)6}.2H2O (M(II) = Mn, Co, Ni) (denoted as MBPO-CJ25) have been synthesized under mild hydrothermal conditions. Single-crystal X-ray diffraction analyses reveal that the three compounds possess isostructural three-dimensional (3D) open frameworks with one-dimensional 12-ring channels along the [001] direction. Notably, the structure can also be viewed as composed of metal phosphate layers [M(II)(PO4)2]4- with Kagomé topology, which are further connected by [B3O7(OH)] triborates, giving rise to a 3D open framework. The guest water molecules locate in the 12-ring channels. Partial Na+ ions reside in the 10-ring side pockets within the wall of the 12-ring channels, and the other Na+ ions and protonated water molecules locate in the 6-ring windows delimited by MO6 and PO4 polyhedra to compensate for the negative charges of the anionic framework. These compounds show a high thermal stability and are stable upon calcinations at ca. 500 degrees C. Ionic conductivities, due to the motion of Na+ ions, are measured for these three compounds. They have similar activation energies of 1.13-1.25 eV and conductivities of 2.7 x 10(-7)-9.9 x 10(-7) S cm(-1) at 300 degrees C. Magnetic measurements reveal that there are very weak antiferromagnetic interactions among the metal centers of the three compounds. Crystal data: MnBPO-CJ25, hexagonal, P6(3)/m (No. 176), a = 11.9683(5) A, c = 12.1303(6) A, and Z = 2; CoBPO-CJ25, hexagonal, P6(3)/m (No. 176), a = 11.7691(15) A, c = 12.112(2) A, and Z = 2; NiBPO-CJ25, hexagonal, P6(3)/m (No. 176), a = 11.7171(5) A, c = 12.0759(7) A, and Z = 2.

Journal Article↗

Clinicopathologic study of parotid involvement in 21 cases of eosinophilic hyperplastic lymphogranuloma (Kimura's disease).

OBJECTIVE: To investigate the clinicopathologic features of eosinophilic hyperplastic lymphogranuloma (Kimura's disease) in the parotid gland. STUDY DESIGN: The hematoxylin and eosin sections and clinical data of 60 patients with eosinophilic hyperplastic lymphogranuloma (Kimura's disease), including with parotid involvement, were reviewed. RESULTS: Of 60 cases of eosinophilic hyperplastic lymphogranuloma (average age, 42 years; average disease duration, 5.8 years), 35 cases (58%) were clinically seen to involve swelling of the parotid region. Parotid specimens were available in 21 cases and showed different microscopic changes. In mildly affected parotid samples, the histological features included infiltration of lymphocytes and eosinophils around the ducts of the interlobular connective tissues. In the moderately involved glands, the infiltrated area was enlarged and contained lymphoid follicles, resulting in adjacent acinar atrophy that was particularly obvious around the salivary ducts. In severe lesions, most acini were lost and only a few ducts remained. All cases with parotid involvement showed more severe pathological changes in the subcutaneous connective tissues and/or local lymph nodes. The parotid lesions often surrounded a central intraglandular lymph node with characteristic features of the disease; however, the salivary parenchyma was left alone. Nerve fibers affected by inflammatory lymphocytes and eosinophils were seen in 38/60 (63%) cases of eosinophilic hyperplastic lymphogranuloma (Kimura's disease) examined in this study. CONCLUSIONS: Eosinophilic hyperplastic lymphogranuloma (Kimura's disease) does not show primary parotid involvement, but instead, pathological changes in the parotid gland are a result of disease spread from the intraparotid lymph nodes and adjacent soft tissues. In addition, our observations suggest that the pruritus often associated with the disease may be due to nerve infiltration by lymphocytes and eosinophils.

Adult↗

Prospective study of 174 de novo acute myelogenous leukemias according to the WHO classification: subtypes, cytogenetic features and FLT3 mutations.

We report a prospective study of 174 unselected adult de novo acute myeloid leukemia (AML) cases diagnosed using the WHO classification. Of those, 57 (33%) were AML with recurrent cytogenetic abnormalities, 41 were (24%) AML with multilineage dysplasia, 74 (42%) were AML not otherwise categorized, and two were acute leukemias of ambiguous lineage. Clonal cytogenetic abnormalities were detected in 64% of the WHO AML cases with t(15;17) (15%), t(8;21) (12%), +8 (11%), -7/del7q (8%) and del9q (5%) being the most common ones. The FLT3/ITD mutations (FMS-like tyrosine kinase 3/internal tandem duplication) were observed in 12% of the WHO AML cases, which is much lower than ones in the literature, while the 6% incidence of the FLT3-activating loop mutations (either FLT3/D835 or FLT3/I836) was comparable with others. Both mutations were associated with leukocytosis. Our study also suggests that the FLT3 mutations are biomarkers independent of cytogenetic characteristics.

Adolescent↗

Protection against avian influenza H9N2 virus challenge by immunization with hemagglutinin- or neuraminidase-expressing DNA in BALB/c mice.

Avian influenza viruses of H9N2 subtype are widely spread in avian species. The viruses have recently been transmitted to mammalian species, including humans, accelerating the efforts to devise protective strategies against them. In this study, an avian influenza H9N2 virus strain (A/Chicken/Jiangsu/7/2002), isolated in Jiangsu Province, China, was used to infect BALB/c mice for adaptation. After five lung-to-lung passages, the virus was stably proliferated in a large quantity in the murine lung and caused the deaths of mice. In addition, we explored the protection induced by H9N2 virus hemagglutinin (HA)- and neuraminidase (NA)-expressing DNAs in BALB/c mice. Female BALB/c mice aged 6-8 weeks were immunized once or twice at a 3-week interval with HA-DNA and NA-DNA by electroporation, respectively, each at a dose of 3, 10 or 30microg. The mice were challenged with a lethal dose (40x LD(50)) of influenza H9N2 virus four weeks after immunization once or one week after immunization twice. The protections of DNA vaccines were evaluated by the serum antibody titers, residual lung virus titers, and survival rates of the mice. The result showed that immunization once with not less than 10microg or twice with 3microg HA-DNA or NA-DNA provided effective protection against homologous avian influenza H9N2 virus.

Animals↗

Determination of vinflunine in rat plasma by liquid chromatography-electrospray ionization mass spectrometry for a pharmacokinetic study.

A rapid, simple and sensitive high-performance liquid chromatography-electrospray ionization mass spectrometry (LC-ESI-MS) method for the quantification of vinflunine in rat plasma was developed and validated. After making alkaline with NaOH, plasma was extracted with ethyl acetate and determined by LC-MS. The analysis was carried out on a Shimadzu VP-ODS column (150 mmx4.6 mm ID, packed with 5 microm C18 Silica RP particle). The mobile phase consisted of methanol-10 mM ammonium acetate buffer (80:20, v/v) with the flow rate of 1.0 ml/min. LC-MS was performed in the selected ion monitoring (SIM) mode using target ions at m/z: 817.3 for vinflunine and m/z: 373.2 for finasteride (IS). Chromatographic separation was achieved in less than 6 min and the calibration curve was linear over a concentration range of 0.025-6.25 microg/ml. The intra-assay and inter-assay variability values were less than 8.6%. The accuracy ranged from 91.5 to 105.6%. The established method has been successfully applied to a pharmacokinetic study of vinflunine in rats.

Animals↗

Extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase pathway is involved in myostatin-regulated differentiation repression.

The cytokines of transforming growth factor beta (TGF-beta) and its superfamily members are potent regulators of tumorigenesis and multiple cellular events. Myostatin is a member of TGF-beta superfamily and plays a negative role in the control of cell proliferation and differentiation. We now show that myostatin rapidly activated the extracellular signal-regulated kinase 1/2 (Erk1/2) cascade in C2C12 myoblasts. A more remarkable Erk1/2 activation stimulated by myostatin was observed in differentiating cells than proliferating cells. The results also showed that Ras was the upstream regulator and participated in myostatin-induced Erk1/2 activation because the expression of a dominant-negative Ras prevented myostatin-mediated inhibition of Erk1/2 activation and proliferation. Importantly, the myostatin-suppressed myotube fusion and differentiation marker gene expression were attenuated by blockade of Erk1/2 mitogen-activated protein kinase (MAPK) pathway through pretreatment with MAPK/Erk kinase 1 (MEK1) inhibitor PD98059, indicating that myostatin-stimulated activation of Erk1/2 negatively regulates myogenic differentiation. Activin receptor type IIb (ActRIIb) was previously suggested as the only type II membrane receptor triggering myostatin signaling. In this study, by using synthesized small interfering RNAs and dominant-negative ActRIIb, we show that myostatin failed to stimulate Erk1/2 phosphorylation and could not inhibit myoblast differentiation in ActRIIb-knockdown C2C12 cells, indicating that ActRIIb was required for myostatin-stimulated differentiation suppression. Altogether, our findings in this report provide the first evidence to reveal functional role of the Erk1/2 MAPK pathway in myostatin action as a negative regulator of muscle cell growth.

Activin Receptors, Type II↗

In vivo disruption of TGF-beta signaling by Smad7 leads to premalignant ductal lesions in the pancreas.

TGF-beta has been postulated to play an important role in the development of pancreatic cancers. More than 50% of human pancreatic cancers bear mutations of Sma- and Mad-related protein (Smad) 4, a critical protein required for TGF-beta signaling. To evaluate the in vivo function of TGF-beta in the development of pancreatic cancers, we generated a transgenic mouse model with pancreas-specific expression of Smad7, a specific inhibitor of TGF-beta signaling. Through the use of elastase I promoter, we directed the tissue specific expression of exogenous Smad7. Consistently, the exogenous Smad7 was detected only in the pancreas in the transgenic mice, and, furthermore, phosphorylation of Smad2 was blocked in the pancreatic tissues. At 6 months of age, most transgenic animals developed premalignant ductal lesions in the pancreas, with characteristics of pancreatic intraepithelial neoplasia (PanIN), a precursor to invasive pancreatic cancers. The premalignant lesions of the pancreas were accompanied by accelerated proliferation of the ductal epithelium and acinar cells, as well as increased fibrosis around the ductal lesions. This study not only demonstrated that in vivo inactivation of TGF-beta signaling is implicated in the development of early stage of pancreatic cancers, but also provided a promising animal model useful for the investigation and intervention of pancreatic cancers in humans.

Animals↗

Role of nitric oxide in Toll-like receptor 2 and 4 mRNA expression in liver of acute hemorrhagic necrotizing pancreatitis rats.

AIM: To investigate the role of nitric oxide (NO) in Toll-like receptor 2 (TLR2)/4mRNA expression in livers of acute hemorrhagic necrotizing pancreatitis (AHNP) rats. METHODS: One hundred and ten SD male rats were randomly divided into sham-operated group (n=10), AHNP group (n=30), chloroquine (CQ)-treated group (n=30) and L-Arg-treated group (n=40). TLR2/4mRNA expression in the liver of AHNP rats was measured by RT-PCR. RESULTS: Expression of TLR2/4mRNA could be detected in the liver of AHNP rats in sham-operated group (0.155E-5+/-0.230E-6 and 0.115E-2+/-0.545E-4), but was markedly increased at 3 h in AHNP group (0.197E-2+/-0.114E-3 and 0.175+/-0.349E-2) peaking at 12 h (0.294E-2+/-0.998E-4 and 2.673+/-2.795E-2, P<0.01). Hepatic injuries were aggravated, TNF-alpha concentration in the liver was increased and NO concentration was decreased (P<0.05 or P<0.01). When TLR2/4mRNA expression was inhibited by CQ (3 h: 1.037E-4+/-3.299E-6 and 0.026+/-3.462E-3; 6 h: 1.884E-4+/-4.679E-6 and 0.108+/-6.115E-3; 12 h: 2.443E-4+/-7.714E-6 and 0.348+/-6.807E-3; P<0.01), hepatic injuries were relieved, NO concentration in the liver was increased and TNF-alpha concentration was decreased (P<0.05 or P<0.01). When rats with AHNP were treated with L-Arg, TLR2/4mRNA expression in the liver could be effectively inhibited (50 mg-T: 0.232E-2+/-0.532E-4 and 0.230+/-6.883E-3; 100 mg-T: 0.210E-2+/-1.691E-4 and 0.187+/-0.849E-2; 200 mg-T: 0.163E-2+/-0.404E-4 and 0.107+/-0.195E-2; 400 mg-T: 0.100E-2+/-0.317E-4 and 0.084+/-0.552E-2; P<0.01) and hepatic injuries were relieved. At the same time, NO concentration in the liver was markedly increased and TNF-alpha concentration was decreased (P<0.05 or P<0.01). CONCLUSION: The expression of TLR2/4mRNA is increased and hepatic injuries are aggravated in the liver of AHNP rats. TLR2/4mRNA gene expression in the liver of AHNP rats can be markedly inhibited by NO, leading to the relief of hepatic injuries.

Alanine Transaminase↗

[Effect of beta-adrenergic agonist on alveolar fluid clearance in acute lung injury: an experiment with rats].

OBJECTIVE: To determine the effect of dobutamine, a beta-adrenergic agonist, on the alveolar fluid clearance (AFC) in acute lung injury (ALI). METHODS: Thirty two male Sprague-Dawley rats were randomly divided into four equal groups: normal control group; ALI group, infused with endotoxin to induce ALI; dobutamine control group, receiving sustained intravenous injection of dobutamine at the dose of 5 microg/kg/min, and dobutamine treatment group, receiving sustained intravenous injection of dobutamine at the dose of 5 microg/kg/min after the administration of endotoxin. Experiment began 45-60 minutes after the circulation was stable. Blood pressure was measured and blood gas analysis was conducted at the beginning of the experiment and one hour later. Perfusion fluid with (125)I-albumin with the radioactivity of 1.5 microCi/ml was perfused into the lung. One hour after the mechanical ventilation the mice were killed and their lungs were taken out. Alveolar fluid was taken out to calculate the AFC by single nuclide tracer technique. RT-PCR was used to detect the expression of alpha, beta, and gamma-rat epithelial sodium channel (rENaC) mRNA. RESULTS: (1) The AFC of ALI group was 14.0 +/- 1.2%, significantly lower than that of the normal control group (21.0 +/- 3.9%, P < 0.05). (2) The AFC of the dobutamine control group was 26.6 +/- 1.6%, significantly higher than that of the normal control group (P < 0.05). and the AFC of the dobutamine treatment group was 20.0 +/- 3.9%, significantly higher than that of the ALI group (P < 0.05). (3) The expression of a-rENaC mRNA was 1.40 +/- 0.40 in the ALI group and was 1.38 +/- 0.13 in the dobutamine treatment group, both significantly higher than those in the dobutamine control group (1.01 +/- 0.14) and in the normal control group (0.44 +/- 0.11, all P < 0.05). The expression of beta-rENaC mRNA was 0.70 +/- 0.8 in the ALI group was 0.71 +/- 0.17 in the dobutamine treatment group, both significantly higher than those in the dobutamine control group (0.58 +/- 0.12) and in the normal control group (0.44 +/- 0.11, all P < 0.05). There were not significant differences in expression of alpha and beta-rENaC mRNA between the normal control group and dobutamine control group, and between the ALI group and dobutamine treatment group (both P > 0.05). (4) The gamma-rENaC mRNA expression was 0.90 +/- 0.19 in the dobutamine control group and was 0.97 +/- 0.15 in the dobutamine treatment group, both significantly higher than that in the normal control group (0.69 +/- 0.10) and in the ALI group (0.70 +/- 0.32) (all P < 0.05). CONCLUSION: Able to upregulate the gamma-rENaC expression and improve the AFC in acute lung injury, beta-adrenergic agonist may be beneficial to reduce lung edema in ALI patients.

Acute Disease↗

Simple determination of pirfenidone in rat plasma via high-performance liquid chromatography.

A simple, rapid and reliable high-performance liquid chromatographic method was developed and validated for the determination of pirfenidone and its major metabolites in rat plasma. Plasma proteins were precipitated with perchloric acid (10%, v/v) and the supernatant after centrifugation was determined using high-performance liquid chromatography. The analysis was carried out on a Lichrospher C(18) column (250 x 4.6 mm i.d., 5 microm). The mobile phase consisted of acetonitrile-water containing 0.2% acetic acid (23:77, v/v) at a flow-rate of 1 mL/min. The eluant was detected at 310 nm. The calibration curves were linear over a concentration range from 0.15 to 76.67 microg/mL. The accuracy (relative error) of the assay ranged from -2.6 to 7.9% and the precision (coefficient of variation) was less than 4.5%. The established method has been successfully applied to a pharmacokinetic study of pirfenidone following a single oral dose to rats.

Animals↗

Stereoselective pharmacokinetics of ornidazole after intravenous administration of individual enantiomers and the racemate.

The pharmacokinetics of ornidazole (ONZ) were investigated following i.v. administration of racemic mixture and individual enantiomers in beagle dogs. Plasma concentrations of ONZ enantiomers were analyzed by chiral high-performance liquid chromatography (HPLC) on a Chiralcel OB-H column with quantification by UV at 310 nm. Notably, the mean plasma levels of (-)-ONZ were higher in the elimination phase than those of (+)-ONZ. (-)-ONZ also exhibited greater t1/2, MRT, AUC(0-t) and smaller CL, than those of its antipode. The area under the plasma concentration-time curve (AUC(0-t)) of (-)-ONZ was about 1.2 times as high as that of (+)-ONZ. (+)-ONZ total body clearance (CL) was 1.4 times than its optical antipode. When given separately, there were significant differences in the values of AUC(0-infinity) and CL between ONZ enantiomers (P < 0.05), indicating that elimination of (+)-ONZ was more rapid than that of (-)-ONZ. No significant differences were found between the estimates of the pharmacokinetic parameters of (+)-ONZ or (-)-ONZ, obtained following administration as the individual and as a racemic mixture. This study demonstrates that the elimination of ONZ enantiomers is stereoselective and chiral inversion and enantiomer/enantiomer interaction do not occur when the enantiomers are given separately and as racemic mixture.

Animals↗

Probing nucleocytoplasmic transport by two-photon activation of PA-GFP.

Two-photon activation of photoactivatable green fluorescent protein (PA-GFP) provides a unique tool for probing cellular transport processes, because activation is strictly limited to the sub-femtoliter optical volume of the two-photon spot. We demonstrate two-photon activation of PA-GFP immobilized in a gel and freely diffusing within cells and recover a quadratic power dependence. Illumination at 820 nm allows simultaneous activation and fluorescence monitoring by two-photon excitation. Alternatively, we activate PA-GFP using two-photon excitation and monitor the fluorescence of the photoconverted product with one-photon excitation. We probe nucleocytoplasmic transport through the nuclear pore complex of COS-1 cells, by observing the time-dependent fluorescence at various locations within the cell after two-photon activation of PA-GFP in the nucleus and in the cytoplasm. Two-photon activation of a tandem construct of two PA-GFPs showed a markedly slower rate of crossing through the nuclear pore. Analysis based on a restricted diffusion model yields a nuclear pore radius of 4.5 nm, which is in good agreement with previously reported values. This application demonstrates the attractive features of two-photon photoactivation over traditional techniques, such as photobleaching, for studying transport processes in cells.

Active Transport, Cell Nucleus↗

Tracing the history of hepatitis B virus genotype D in western Japan.

The major hepatitis B virus (HBV) genotypes in Japan are B and C. HBV genotype D (HBV/D), however, is widespread in a small area of Western Japan, where the Gianotti-Crosti syndrome caused by HBV subtype ayw, which is suspected to be HBV/D, was endemic in the 1970s. The aim of the study was to elucidate its origin, time of transmission, and spread in this area. Genotyping of HBV-DNA was done in 363 patients with HBV infection. The year of birth was checked in patients with HBV/D. The full genome sequences of 20 HBV/D strains, 2 of which were obtained from a single carrier with a 19-year-interval, were analyzed. An evolutionary rate, the date of the most recent common ancestor, and the effective number of HBV/D infections were calculated. Fifty-two of 363 patients were infected with HBV/D, and 39 were born in 1970s. In a phylogenetic tree, the 20 HBV/D strains produced a definite cluster, and the evolutionary rate was calculated to be 5.4 x 10(-5) nucleotide substitutions/site/year. The root of the tree was estimated to be in approximately 1,900 and began to spread from the 1940s, leading to a rapid increase of infected patients in the 1970s. From these results, it is suspected that HBV/D was likely transmitted to the area investigated approximately 100 years ago and then spread widely in the 1970s. From the history of the area and the genetic analysis, HBV/D in this area was speculated to be of Russian origin.

Acrodermatitis↗

HDAC1 expression and effect of curcumin on proliferation of Raji cells.

Histone deacetylase (HDAC1) has a high expression in many cancer cells and curcumin can inhibit the growth of cancer cells. This paper was designed to investigate the expression of HDAC1 of Raji cells and the effect of curcumin on their proliferation and apoptosis. Raji cells were treated with 3.125-50 micromol/L curcumin for 8-48 h and the growth inhibition rates of Raji cells were measured by MTT. The expression of HDAC1 on Raji cells were examined by mRNA, Western blot at 24 h various concertrations (1.6-50 micromol/L). Curcumin could selectively inhibit the proliferation of Raji cells in a dose- and time-dependent manner, with the inhibition rate being 52.47 %-82.18 % (P<0.01). The up-regulation of HDAC1 expression was observed within 24 h after the treatment with curcumin as shown by RT-PCR and Western blot. With the increase of concentration, the expression was down-regulated in a dose- dependent manner. It is concluded that the expression of HDAC1 plays an important role in the proliferation and apoptosis of Raji cells and curcumin can inhibit the growth of Raji cells at various concentrations and promote the apoptosis of Raji cells.

Antineoplastic Agents, Phytogenic↗